K E Y W O R D S : 2-hydroxyethyl methacrylate, baseline series, patch test Positive reactions, n (%) Relevant positive reactions, n (%) Non-relevant positive reactions, n (%) No. of patients (%) + ++ +++ No. of patients (%) + ++ +++ No. of patients (%) + ++ +++ Total: 61 (1.5)

Female pattern hair loss, also known as female androgenetic alopecia, is generally regarded as an androgen-dependent disorder representing the female counterpart of male balding. We describe female pattern hair loss occurring in a patient with complete androgen insensitivity syndrome suggesting that mechanisms other than direct androgen action contribute to this common form of hair loss in women.Women with female pattern hair loss (FPHL) typically present with a history of gradual thinning of scalp hair, often over a period of several years. On examination they show widening of the central parting with a diffuse reduction in hair density mainly affecting the frontal scalp and crown. The frontal hairline is usually retained. FPHL is common, affecting about 5% of women by the age of 50 years increasing to over 30% by age 70. 1,2 The underlying change in hair follicle physiology is progressive miniaturization in a proportion of hair follicles, shortening of the growth phase of the hair cycle (anagen) and prolongation of the resting phase (telogen). 3,4 FPHL has long been thought to be the female counterpart of male balding and is often referred to as female androgenetic alopecia. However, the role of androgens in FPHL is less clear-cut than in male balding. We report a case of FPHL that reinforces this uncertainty and implicates androgen-independent mechanisms in the pathogenesis. Case reportA 52-year-old woman presented with a 10-year history of gradual thinning of her scalp hair. On examination she had a diffuse reduction in hair density affecting the mid and frontal regions of the scalp with retention of the frontal hair line (Fig. 1). The scalp appeared normal with no evidence of scarring. The clinical features were typical of FPHL of Ludwig grade I. Several years previously she had been diagnosed with complete androgen insensitivity syndrome (CAIS) following investigation of primary amenorrhoea. Her sister has the same condition but without hair loss. On general examination she had normal female external genitalia and breast development with scanty pubic hair but no axillary hair or beard growth. Chromosome analysis showed a 46XY karyotype. Intra-abdominal testes were found on ultrasound examination. She had high circulating levels of testosterone (28AE1 nmol L )1 , normal male range 8-28) and dihydrotestosterone (3AE9 nmol L )1 , normal male range 0AE9-2AE9). Thyroid-stimulating hormone and free thyroxine levels were normal. Her serum estradiol was in the lower normal range for a woman of reproductive age (142 pmol L )1 ). She continues to be monitored by the gynaecologists with regular ultrasound scans and tumour marker evaluation as she has refused orchiectomy. Androgen receptor gene analysis was also declined by the patient.Prior to referral she had tried topical minoxidil and oestrogen replacement therapy, both for 12 months, with no improvement in hair density. Oral finasteride (dose range 1AE25-2AE5 mg daily) and spironolactone (maximum dose 300 mg daily) were also ineffective. Some improvement was notic...

SummaryThere are concerns about the induction of metal allergy with second-generation metalon-metal prostheses, and the role that this may play in the development of complications such as 'pseudotumours' or failure of the implant. In this review, we attempt to set out the current knowledge on this subject. From a review of the literature, it is apparent that the first-generation metal-on-metal replacement hips did cause metal sensitization, and that joint failure was associated with this, although it is still not clear which one led to the other. Highly engineered second-generation metal-on-metal arthroplasties used in joint resurfacings are now increasingly employed. Several studies have recently shown an association between metal sensitization and peri-implant hypersensitivity reactions and implant loosening and failure, although the overall risk appears to be low. The pragmatic approach adopted by most contact dermatologists for patients known to be allergic to nickel, cobalt or chromium and who require joint replacement is to recommend prostheses made of titanium-based alloys. Patch testing continues to be a useful tool as laboratory investigations for metal hypersensitivity continue to emerge. The development of guidelines on the management of patients receiving metal-on-metal arthroplasties suspected of being metal-allergic is desirable.Key words: metal allergy; nickel; prosthesis failure; pseudotumour; second-generation arthroplasty.Second-generation metal-on-metal arthroplasties are increasingly used, especially in younger patients, but questions about metal sensitivity and its role in pseudotumour formation and implant failure have arisen. The development of the new type of metal-on-metal prosthesis over the last decade resulted from the acknowledgement of the ability of plastic-wear particles from metal-on-plastic prostheses to produce a foreign body reaction in the tissues surrounding the joint (with the potential consequence of aseptic loosening of the prosthesis) coupled with improvements in bioengineering (1). These second-generation metal-on-metal prostheses involve less invasive surgery, are better engineered, with a narrower joint space, and are associated with lower rates of wear debris.

References1 McFadden JP, Baker BS, Powles AV, Fry L. Psoriasis and streptococci: the natural selection of psoriasis revisited. Br J Dermatol 2009; 160:929-37. 2 Ting KM, Rothaupt D, McCormick TS et al. Overexpression of the oncofetal Fn variant containing the EDA splice-in segment in the dermal-epidermal junction of psoriatic uninvolved skin. J Invest Dermatol 2000; 114:706-11. 3 Manabe R, Oh-e N, Sekiguchi K. Alternatively spliced EDA segment regulates fibronectin-dependent cell cycle progression and mitogenic signal transduction. J Biol Chem 1999; 274:5919-24. 4 Bata-Csorgo Z, Cooper KD, Ting KM et al. Fibronectin and alpha5 integrin regulate keratinocyte cell cycling. A mechanism for increased fibronectin potentiation of T cell lymphokine-driven keratinocyte hyperproliferation in psoriasis. J Clin Invest 1998; 101:1509-18.5 Lasarte JJ, Casares N, Gorraiz M et al. The extra domain A from fibronectin targets antigens to TLR-4 expressing cells and induces cytotoxic T cell responses in vivo. J Immunol 2007; 178:748-56. 6 Su S-L, Tsai C-D, Lee C-H et al. Expression and regulation of Toll-like receptor 2 by IL-b and fibronectin fragments in human articular chondrocytes. Osteoarthritis Cartilage 2005; 13:879-86. 7 Lyakh L, Trinchieri G, Provezza L et al. Regulation of interleukin-12 ⁄ interleukin-23 production and the T-helper 17 response in humans. Immunol Rev 2008; 226:112-31. 8 Späh F. Inflammation in atherosclerosis and psoriasis: common pathogenic mechanisms and the potential for an integrated treatment approach. Br J Dermatol 2008; 159 (Suppl. 2):10-17. 9 White ES, Baralle FE, Muro AF. New insights into form and function of fibronectin splice variants. J Pathol 2008; 216:1-14. 10 Schoneveld AH, Hoefer I, Sluitjer JP et al. Atherosclerotic development and Toll like receptor 2 and 4 responsiveness. Atherosclerosis 2008; 197:95-104.common among dermatology patients. It is important to be aware of the effects of melanotan on pre-existing MN and as a trigger for new MN. Our patient experienced both. We submitted our case as the first report in the dermatology literature on eruptive naevi following melanotan injections. Since then, a case of eruptive naevi after self-administration of synthetic a-MSH has been published. 6 References 1 Evans-Brown M, Dawson RT, Chandler M, McVeigh J. Use of melanotan I and II in the general population. BMJ 2009; 338:b566.

The varying prevalences of polysensitization across Europe most likely reflect differences in patient characteristics and referral patterns between departments. Known risk factors for polysensitization are confirmed in a European dermatitis population.